Relevant bibliographies by topics / Atherosclerosis – Risk factors

Contents

  1. Journal articles
  2. Dissertations / Theses
  3. Books
  4. Book chapters
  5. Conference papers

Academic literature on the topic 'Atherosclerosis – Risk factors'

Author: Grafiati
Published: 4 June 2021
Last updated: 28 January 2023

Create a spot-on reference in APA, MLA, Chicago, Harvard, and other styles

Select a source type:

Consult the lists of relevant articles, books, theses, conference reports, and other scholarly sources on the topic 'Atherosclerosis – Risk factors.'

Next to every source in the list of references, there is an 'Add to bibliography' button. Press on it, and we will generate automatically the bibliographic reference to the chosen work in the citation style you need: APA, MLA, Harvard, Chicago, Vancouver, etc.

You can also download the full text of the academic publication as pdf and read online its abstract whenever available in the metadata.

Journal articles on the topic "Atherosclerosis – Risk factors"

1

FUJITA, Toshiro, and Katsuyuki ANDO. "Risk Factors of Atherosclerosis." Journal of Japan Atherosclerosis Society 23, no. 7-8 (1996): 423–27. http://dx.doi.org/10.5551/jat1973.23.7-8_423.

Full text
APA, Harvard, Vancouver, ISO, and other styles
2

Siscovick, David, Frits Rosendaal, and Alexander Reiner. "Hemostatic Risk Factors and Arterial Thrombotic Disease." Thrombosis and Haemostasis 85, no. 04 (2001): 584–95. http://dx.doi.org/10.1055/s-0037-1615638.

Full text
Abstract:
SummaryThe pathogenesis of arterial thrombotic disease involves multiple genetic and environmental factors related to atherosclerosis and thrombosis. Acute thrombosis at the site of a ruptured, lipid-rich atherosclerotic plaque is the usual precipitating event in the transition from stable or subclinical atherosclerotic disease to acute myocardial infarction (MI), stroke, or peripheral arterial occlusion (1). Pathologic studies of coronary arteries in acute MI suggest that the acute thrombosis likely involves activation of both platelets and the coagulation system.
APA, Harvard, Vancouver, ISO, and other styles
3

D’Adamo, Ebe, Ornella Guardamagna, Francesco Chiarelli, Andrea Bartuli, Daniela Liccardo, Federica Ferrari, and Valerio Nobili. "Atherogenic Dyslipidemia and Cardiovascular Risk Factors in Obese Children." International Journal of Endocrinology 2015 (2015): 1–9. http://dx.doi.org/10.1155/2015/912047.

Full text
Abstract:
Childhood obesity when associated with serum lipoprotein changes triggers atherosclerosis. Evidences suggest that the atherosclerotic process begins in childhood and that the extent of early atherosclerosis of the aorta and coronary arteries can be associated with lipoprotein levels and obesity. Furthermore, many studies in childhood demonstrate an important relationship between parameters of insulin sensitivity, body fat distribution, and the development of lipid abnormalities. This review focuses on the most recent findings on the relationship between obesity, dyslipidemia, and cardiovascular risk in children.
APA, Harvard, Vancouver, ISO, and other styles
4

YASUDA, Hideaki, Hideyuki TSUBOI, and Takahito SONE. "Risk factors influencing carotid atherosclerosis." Choonpa Igaku 34, no. 1 (2007): 57–63. http://dx.doi.org/10.3179/jjmu.34.57.

Full text
APA, Harvard, Vancouver, ISO, and other styles
5

Kullo, Iftikhar J., Gerald T. Gau, and A. Jamil Tajik. "Novel Risk Factors for Atherosclerosis." Mayo Clinic Proceedings 75, no. 4 (April 2000): 369–80. http://dx.doi.org/10.4065/75.4.369.

Full text
APA, Harvard, Vancouver, ISO, and other styles
6

Kullo, Iftikhar J., and Christie M. Ballantyne. "Conditional Risk Factors for Atherosclerosis." Mayo Clinic Proceedings 80, no. 2 (February 2005): 219–30. http://dx.doi.org/10.4065/80.2.219.

Full text
APA, Harvard, Vancouver, ISO, and other styles
7

Dobroski, David R., and Joseph Loscalzo. "Thrombotic risk factors for atherosclerosis." Coronary Artery Disease 7, no. 12 (December 1996): 919–32. http://dx.doi.org/10.1097/00019501-199612000-00007.

Full text
APA, Harvard, Vancouver, ISO, and other styles
8

Leijdekkers, V. J., A. C. Vahl, J. J. M. Leenders, P. C. Huijgens, R. O. B. Gans, and J. A. Rauwerda. "Risk Factors for Premature Atherosclerosis." European Journal of Vascular and Endovascular Surgery 17, no. 5 (May 1999): 394–97. http://dx.doi.org/10.1053/ejvs.1998.0775.

Full text
APA, Harvard, Vancouver, ISO, and other styles
9

Rosanov, V., E. Shugaeva, A. Alexandrov, and Ch Pugoeva. "Alimentary risk factors of atherosclerosis." Atherosclerosis Supplements 2, no. 2 (May 2001): 112. http://dx.doi.org/10.1016/s1567-5688(01)80311-1.

Full text
APA, Harvard, Vancouver, ISO, and other styles
10

Papazafiropoulou, Athanasia, Nicholas Katsilambros, and Nicholas Tentolouris. "Novel Risk Factors for Atherosclerosis." Open Biomarkers Journal 1, no. 1 (December 5, 2008): 36–47. http://dx.doi.org/10.2174/1875318300801010036.

Full text
Abstract:
Epidemiologic studies demonstrated that the classical cardiovascular risk factors explain only a part of the increased cardiovascular morbidity and mortality. Large scale studies have shown that novel cardiovascular risk factors, including increased plasma homocysteine, fibrinogen, C-reactive protein, uric acid levels, and increased white blood cells count as well as low adiponectin levels, might have a key role in the pathogenesis of the cardiovascular disease. This review examines recent literature data on the effect of novel risk factors on cardiovascular morbidity and mortality in healthy subjects as well as in subjects at high cardiovascular risk. In addition, the pathogenetic mechanisms linking the effects of the novel risk factors with atherosclerosis are discussed.
APA, Harvard, Vancouver, ISO, and other styles
More sources

Dissertations / Theses on the topic "Atherosclerosis – Risk factors"

1

Persson, Jerker. "Ultrasound and atherosclerosis evaluation of methods, risk factors and intervention /." Malmö : Lund : Malmö University Hospital ; Lund University, 1997. http://catalog.hathitrust.org/api/volumes/oclc/68945104.html.

Full text
APA, Harvard, Vancouver, ISO, and other styles
2

Pöykkö, S. (Seppo). "Ghrelin, metabolic risk factors and carotid artery atherosclerosis." Doctoral thesis, University of Oulu, 2005. http://urn.fi/urn:isbn:9514276566.

Full text
Abstract:
Abstract The increasing prevalence of metabolic syndrome and the consequent cardiovascular diseases, including atherosclerotic diseases and type 2 diabetes, are a cause of public concern worldwide. This development has stimulated an active search for novel risk factors and new candidate genes. The hormones regulating energy balance and the polymorphisms associated with them are of special interest as potential risk factors for metabolic syndrome. Ghrelin is a novel peptide hormone from stomach with strong growth hormone releasing activity. It is also able to modify glucose and insulin metabolism, blood pressure levels, cardiac function, adipogenesis and inflammatory processes in experimental conditions. Whether ghrelin and ghrelin gene variations have a role in the development of metabolic syndrome and the associated diseases, is not known. In the present study, the associations between fasting plasma ghrelin concentrations, ghrelin gene mutations (Arg51Gln and Leu72Met), features of metabolic syndrome, type 2 diabetes and carotid artery atherosclerosis were analysed. In addition, the relationship between ghrelin and insulin-like growth factor I (IGF-I) concentrations was studied. The study population consisted of 1045 middle-aged subjects of the hypertensive and the control cohorts of the OPERA project from the City of Oulu, Finland. Low ghrelin concentrations were found to be associated with several components of metabolic syndrome: adiposity, low HDL cholesterol levels, high insulin concentrations and high blood pressure levels. The prevalence of insulin resistance and type 2 diabetes was increased amongst the subjects with low ghrelin concentrations. Out of the individual factors tested, IGF-I concentration was the most significant predictor of ghrelin concentrations. This negative association was strongest in the subjects with insulin resistance and type 2 diabetes, which suggests that changes in ghrelin/IGF-I interactions might be involved in the development of these conditions. The subjects with the Gln51 allele of the ghrelin gene had lower ghrelin concentrations and, consistent with the findings mentioned above, higher prevalence of type 2 diabetes and hypertension compared with the subjects homozygous for the Arg51 allele. No correlation between ghrelin and C-reactive protein concentrations was seen. However, there was a positive association between ghrelin concentrations and carotid artery intima-media thickness. This association was independent of the commonly recognised risk factors of atherosclerosis and was only seen in men, who also had more advanced atherosclerosis than women. These observations call for further studies to clarify the potential causative role of ghrelin in the etiology of metabolic syndrome, type 2 diabetes and atherosclerotic cardiovascular diseases
Tiivistelmä Metaboliseen oireyhtymään liittyy kohonnut riski sairastua sydän- ja verisuonisairauksiin kuten tyypin 2 diabetekseen ja sepelvaltimotautiin. Metabolisen oireyhtymän nopea esiintyvyyden kasvu on johtanut aktiiviseen uusien riskitekijöiden etsintään. Erityisen kiinnostuksen kohteena ovat olleet energia-aineenvaihduntaa säätelevät hormonit ja niihin liittyvät polymorfiat. Greliini on ensisijaisesti vatsalaukusta erittyvä hormoni, joka lisää voimakkaasti kasvuhormonin eritystä. Koeolosuhteissa sillä on myös vaikutuksia sokeriaineenvaihduntaan, verenpaineeseen, sydämen toimintaan, rasvakudoksen kehittymiseen ja tulehduksellisiin tapahtumiin, minkä perusteella on syytä epäillä greliinillä olevan osuutta metabolisen oireyhtymän ja siihen liittyvien sairauksien synnyssä. Tässä tutkimuksessa selviteltiin greliinin paastoplasmapitoisuuksien ja greliinipolymorfioiden (Arg51Gln ja Leu72Met) yhteyksiä metabolisen oireyhtymän piirteisiin, tyypin 2 diabetekseen ja kaulavaltimoiden ateroskleroosiin. Lisäksi tutkittiin greliinin ja insuliinin kaltaisen kasvutekijän (IGF-I) pitoisuuksien yhteyksiä. Tutkimusväestö koostui 1045 oululaisesta keski-ikäisestä OPERA tutkimukseen kuuluvasta henkilöstä. Tutkimuksessa matalien greliinipitoisuuksien havaittiin olevan yhteydessä useisiin metabolisen oireyhtymän piirteisiin: lihavuuteen, alhaisiin HDL kolesterolin pitoisuuksiin, korkeisiin insuliinipitoisuuksiin ja kohonneeseen verenpaineeseen. Matala greliinipitoisuus yhdistyi myös tyypin 2 diabeteksen ja verenpainetaudin esiintyvyyteen. Tutkituista tekijöistä IGF-I -pitoisuudet selittivät parhaiten greliinipitoisuuksia. Tämä käänteinen yhteys oli erityisen vahva tyypin 2 diabeetikoilla ja insuliiniresistenteillä henkilöillä viitaten greliinin ja IGF-I:n mahdollisen vuorovaikutukseen liittyvän näiden tilojen kehittymiseen. Lisäksi havaittiin, että greliinigeenin Gln51-alleelia kantavien henkilöiden greliinipitoisuudet olivat alhaiset, ja että he sairastivat enemmän diabetesta ja verenpainetautia kuin henkilöt jotka olivat homotsygootteja Arg51-alleelin suhteen. Greliinipitoisuudet ja C-reaktiivisen proteiinin pitoisuudet eivät korreloineet keskenään. Kaulavaltimon seinämäpaksuus korreloi positiivisesti greliinipitoisuuksien kanssa miehillä riippumatta perinteisistä ateroskleroosin riskitekijöistä. Tutkimustulokset tukevat olettamusta, että greliinillä saattaa olla merkitystä metabolisen oireyhtymän, tyypin 2 diabeteksen ja ateroskleroosin kehittymisessä. Jatkotutkimukset ovat tarpeen tämän yhteyden osoittamiseksi
APA, Harvard, Vancouver, ISO, and other styles
3

Rerkasem, Kittipan. "The risk factors associated with carotid artery disease." Thesis, University of Southampton, 2002. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.271581.

Full text
APA, Harvard, Vancouver, ISO, and other styles
4

Xu, Lin, and 徐琳. "Subclinical atherosclerosis, cardiovascular risk factors and metabolicsyndrome in older Chinese people." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2010. http://hub.hku.hk/bib/B4451430X.

Full text
APA, Harvard, Vancouver, ISO, and other styles
5

Rantala, M. (Maire). "Dietary modification and genetic variability of atherosclerosis risk factors." Doctoral thesis, University of Oulu, 2000. http://urn.fi/urn:isbn:9514256522.

Full text
Abstract:
Abstract The risk factors for atherosclerosis and coronary heart disease (CHD) are multiple and may interact with each other. Diet has a significant role among the main risk factors for atherosclerosis, as it regulates the levels of plasma lipids and lipoproteins, their oxidative modification or protection from oxidation, blood pressure, energy balance, and thrombogenesis. Nutrients can transfer their effects directly through plasma concentrations or modify the cell transduction or gene expression of important regulatory genes. The response to dietary modification varies between individuals. The plasma cholesterol response induced by dietary modification is at least partly regulated genetically and some of the variation is explained by other environmental factors. Apolipoprotein E (apo E) and apolipoprotein B (apo B) are the key regulatory proteins in cholesterol and lipoprotein metabolism. The genetic variation of apo E is associated with the plasma lipid levels and the CHD risk. The polymorphic variation of the apo B gene is also associated with increased plasma cholesterol and CHD risk. Obesity is associated with increased morbidity and mortality. Plasma lipid abnormalities, impaired glucose metabolism and increased blood pressure caused by obesity are the main reasons for increased CHD mortality among obese subjects. To study the magnitude of the response to dietary modification, genetically selected groups were investigated. Dietary modification had a significant impact on plasma total, LDL, and HDL cholesterol concentrations, and the individual response in plasma LDL cholesterol varied from 3 to 100%. The role of genetic variation in the apo E gene was not significant in the lipid response, but the blood pressure response was more distinct among subjects with the ε 4 allele than those with the ε 3 allele. The determination of apo B EcoRI and MspI gene polymorphisms revealed subjects with a greater response to diet, a finding which may have clinical importance in the future for the attempt to identify subjects for effective dietary counselling. The effect of caloric restriction on gene expression was studied in obese gallstone patients. Moderate weight reduction during caloric restriction was associated with reduced lipoprotein lipase gene expression, while the cholesteryl ester transfer protein gene expression remained unchanged. Some of the beneficial changes in plasma lipids and lipoproteins during and after weight reduction may be followed by altered transcription of their modifying genes. Meta-analysis is a modern and generally accepted method. Many clinical uncertainties can be solved by combining all the data available to a quantitative and objective analysis. However, the use of meta-analysis do not resolve the problem of the effect of publication bias.
APA, Harvard, Vancouver, ISO, and other styles
6

Karvonen, J. (Jarkko). "Genetic and immunological risk factors and carotid artery atherosclerosis." Doctoral thesis, University of Oulu, 2004. http://urn.fi/urn:isbn:9514272609.

Full text
Abstract:
Abstract Atherosclerosis is a multifactorial disease with numerous genes and environmental factors affecting its intiation and progression. During the past years many candidate genes for atherosclerosis have been suggested, and it has also become evident that the immune system plays a part in atherogenesis. Early atherosclerotic changes can be effectively detected by measuring carotid artery intima-media thickness (IMT). In the present study the associations between IMT and polymorphisms of three candidate genes for atherosclerosis were studied: endothelial nitric oxide synthase (eNOS), apolipoprotein E (apoE) and paraoxonase-1 (PON1). To assess the role of immunological factors determining carotid atherosclerosis, CRP and circulating autoantibodies to oxidised LDL were studied in relation to IMT. The study population consisted of 519 hypertensive and 526 control subjects from a middle-aged population in Oulu, Finland. The results showed that the investigated polymorphisms of eNOS and PON1 genes were not associated with IMT, suggesting that these polymorphisms are not major risk factors for atherosclerosis in the general Caucasian population. A significant interaction between the apoE polymorphism and smoking in relation to IMT was observed among men, indicating that carriers of the ε4 allele may be particularly prone to the atherogenic effects of smoking. This interaction was especially clear in hypertensive subjects. CRP was strongly associated with IMT before adjusting for confounding factors. After the adjustment, this association diasppeared. The finding suggests that instead of early atherosclerosis CRP may be related to the later phases of the disease. This may partly explain the strong correlation between CRP and future cardiovascular events. IgM type of autoantibodies binding to oxidised LDL were inversely associated with IMT, and this finding remained after adjusting for previously known risk factors for atherosclerosis, implying a possible protective role for these antibodies in atherogenesis.
APA, Harvard, Vancouver, ISO, and other styles
7

Hietaniemi, M. (Mirella). "Studies on novel and traditional risk factors of atherosclerosis." Doctoral thesis, University of Oulu, 2009. http://urn.fi/urn:isbn:9789514291296.

Full text
Abstract:
Abstract The atherosclerotic plaques develop with the adhesion of inflammatory cells and lipids onto the innermost layer of the vessel. They may eventually occlude the vessel impairing blood flow. A severe complication is the rupture of a plaque resulting in the formation of a thrombus that can cause myocardial infarction or stroke. Though a large number of risk factors for atherosclerosis have been identified, the pathogenesis of atherosclerosis is far from unravelled. The aim of the present work was to study both traditional as well as potential novel risk factors of atherosclerosis. The first study examined the relationship between IGF-I concentrations and carotid artery atherosclerosis and its metabolic risk factors. Low IGF-I concentrations were associated with several cardiovascular risk factors. A positive association was observed between IGF-I concentrations and carotid artery intima-media thickness in women. The results suggest that IGF-I may be involved in the pathogenesis of atherosclerosis. Interestingly, the effect may manifest differentially in men and women. The second study focused upon the effects of obesity and weight loss on liver gene expression. A global decrease in gene expression was observed. The down-regulated genes included genes involved in the ubiquitin cycle, which may point to a reduction in oxidative stress due to the hypocaloric diet. The down-regulation of peroxisome proliferator-activated receptor gamma cofactor 1 alpha (PGC-1α) may be related to improved insulin sensitivity. Several novel genes not previously linked to obesity and weight loss were also discovered. In the third and fourth studies, the developmental origins of atherosclerosis hypothesis was studied in a rat model of fetal undernutrition. Unfavourable changes in the obesity-related peptide hormones adiponectin and resistin were observed which could predispose to insulin resistance in later life. In addition, total cholesterol levels were elevated in the undernourished offspring. The gene expression changes in the rat pups suggest that the development of pancreas was affected, which might further contribute to disturbances in insulin and glucose metabolism
Tiivistelmä Ateroskleroosi eli valtimonkovettumatauti on sairaus, joka saa alkunsa verisuonen sisäseinämään kiinnittyvistä tulehdussoluista ja veren rasvapartikkeleista, joista muodostuu pitkän ajan kuluessa ateroskleroottisia plakkeja. Plakit voivat kasvaessaan heikentää veren virtausta valtimoissa ja pahimmillaan jopa tukkia suonen kokonaan. Mikäli plakki repeää, voi muodostua verihyytymä joka sydämessä aiheuttaa sydäninfarktin ja aivoissa aivoinfarktin. Vaikka useita ateroskleroosille altistavia tekijöitä tunnetaan, taudin syntymekanismit ovat vielä suurelta osin selvittämättä. Tämän väitöskirjatyön tarkoituksena oli tutkia sekä ateroskleroosin perinteisiä että mahdollisia uusia riskitekijöitä. Ensimmäisessä osatyössä tutkittiin insuliininkaltaisen kasvutekijä I:n (IGF-I) yhteyttä kaulavaltimon ateroskleroosiin sekä perinteisiin ateroskleroosin riskitekijöihin. Matalat IGF-I pitoisuudet liittyivät moniin ateroskleroosin riskitekijöihin. Naisissa korkeammat IGF-I pitoisuudet kuitenkin yhdistyivät paksumpaan kaulavaltimoon, mikä viittaa ateroskleroosiin. Tulosten perusteella IGF-I saattaa liittyä ateroskleroosin kehitykseen ja mahdollisesti sen vaikutukset ilmenevät naisissa ja miehissa eri tavoin. Toisessa osatyössä tutkittiin maksan geenien ilmentymistä lihavuudessa ja laihdutusjakson jälkeen. Laihduttaneessa ryhmässä 142:n geenin ilmentyminen oli vähentynyt ja vain yhden lisääntynyt suhteessa kontrolliryhmään. Ubikitiini-syklin geenien ilmentymisen väheneminen voi viitata vähentyneeseen oksidatiiviseen stressiin elimistössä dieetin seurauksena. Muun muassa diabetekseen liittyvän geenin, peroxisome proliferator-activated receptor gamma cofactor 1 alpha, väheneminen puolestaan voi liittyä parantuneeseen insuliiniherkkyyteen laihduttaneissa. Lisäksi tässä työssä tuli esiin monia uusia, mielenkiintoisia geenejä, joita ei aiemmin ole yhdistetty lihavuuteen tai ateroskleroosiin. Kolmannessa ja neljännessä osatyössä selvitettiin ns. Barkerin hypoteesia, eli sitä, voisiko sairastumisalttius määräytyä jo sikiökauden ja varhaiskehityksen aikana. Rottakokeemme osoittivat, että sikiöaikaisen aliravitsemuksen seurauksena kolesteroliarvot olivat korkeammat ja että lihavuuteen liittyvien peptidihormonien, adiponektiinin ja resistiinin, pitoisuuksissa oli tapahtunut epäsuotuisia muutoksia, jotka voivat altistaa insuliiniresistenssille Tulokset viittasivat myös siihen, että aliravitsemus oli mahdollisesti vaikuttanut haiman kehitykseen, mikä voi myös osaltaan vaikuttaa mm. insuliini- ja sokeriaineenvaihduntaan. Tämänkaltaiset muutokset saattavat altistaa ateroskleroosille myöhemmällä iällä
APA, Harvard, Vancouver, ISO, and other styles
8

Rantala, A. (Asko). "Risk factors and carotid atherosclerosis in hypertensive and control subjects." Doctoral thesis, University of Oulu, 2001. http://urn.fi/urn:isbn:9514264657.

Full text
Abstract:
Abstract Different metabolic and environmental factors affect the blood pressure level, constituting a cluster, especially in hypertensives, that leads to an increased risk of cardiovascular diseases. The present research was designed to determine the prevalence and the predictors of the metabolic syndrome and the role of insulin and blood pressure in carotid atherosclerosis in 600 treated male and female hypertensives aged 40-59 years and 600 age- and sex-matched controls. The prevalence of the metabolic syndrome in different population-based cohorts varied, depending on the definition, from 0.8% to 35.3%, being lowest in control men and women and highest in hypertensive men. 73.8% of a random, middle-aged, urban population showed at least one cardiovascular risk factor, and 91.3% of all hypertensive subjects showed at least one cardiovascular risk factor in addition to hypertension itself. The independent predictors of the metabolic syndrome were waist circumference, uric acid, total cholesterol and gamma-glutamyl transpeptidase. Hypertension had a significant effect on carotid intima-media thickness and the prevalence of plaques in men, but its effect in women was not significant. A long duration of hypertension resulted in greater intima-media thickness and a higher prevalence of plaques, particularly in men. There were significant associations between gamma-glutamyl transpeptidase and the components of the metabolic syndrome after adjustment for alcohol consumption and also in teetotallers. There were inconsistent associations between the different insulin measures and the intima-media thickness as a measure of carotid atherosclerosis. The exclusion of diabetic subjects did not change the results. In conclusion, a cluster of metabolic abnormalities related to hypertension is frequent among both controls and treated hypertensive subjects. Hypertensive subjects have higher prevalences of carbohydrate and lipoprotein aberrations and structural and functional cardiovascular complications than age- and sex-matched controls.
APA, Harvard, Vancouver, ISO, and other styles
9

Nicoll, Rachel. "Insights into the relationship between coronary calcification and atherosclerosis risk factors." Doctoral thesis, Umeå universitet, Institutionen för folkhälsa och klinisk medicin, 2016. http://urn.kb.se/resolve?urn=urn:nbn:se:umu:diva-124909.

Full text
Abstract:
Introduction Coronary artery disease (CAD) is the most common cause of death in Europe and North America and early detection of atherosclerosis is a clinical priority. Diagnosis of CAD remains conventional angiography, although recent technology has introduced non-invasive imaging of coronary arteries using computed tomographic coronary angiography (CTCA), which enables the detection and quantification of coronary artery calcification (CAC). CAC forms within the arterial wall and is usually found in or adjacent to atherosclerotic plaques and is consequently known as sub-clinical atherosclerosis.  The conventional cardiovascular (CV) risk factors used to quantify the estimated 10-year coronary event risk comprise dyslipidaemia, hypertension, diabetes mellitus, obesity, smoking and family history of CAD. Nevertheless, their relationship with significant (>50%) stenosis, their interaction with the CAC score and their predictive ability for CAC presence and extent has not been fully determined in symptomatic patients.   Methods   For Papers 1-4 we took patients from the Euro-CCAD cohort, an international study established in 2009 in Umeå, Sweden. The study data gave us the CAC score and the CV risk factor profile in 6309 patients, together with angiography results for a reduced cohort of 5515 patients. In Papers 1 and 2 we assessed the risk factors for significant stenosis, including CAC as a risk factor. Paper 2 carried out this analysis by geographical region: Europe vs USA and northern vs southern Europe. Paper 3 investigated the CV risk factors for CAC presence, stratified by age and gender, while Paper 4 assessed the CV risk factors for CAC extent, stratified by gender.  In paper 5 we carried out a systematic review and meta-analysis of all studies of the risk factor predictors of CAC presence, extent and progression in symptomatic patients. From a total of 884 studies, we identified 10 which fitted our inclusion criteria, providing us with a total of 15,769 symptomatic patients. All 10 were entered in the systematic review and 7 were also eligible for the meta-analysis.   Results Paper 1:           Among risk factors alone, the most powerful predictors of significant coronary stenosis were male gender followed by diabetes, smoking, hypercholesterolaemia, hypertension, family history of CAD and age; only obesity was not predictive. When including the log transformed CAC score as a risk factor, this proved the most powerful predictor of >50% stenosis, but hypercholesterolaemia and hypertension lost their predictive ability. The conventional risk factors alone were 70% accurate in predicting significant stenosis, the log transformed CAC score alone was 82% accurate but the combination was 84% accurate and improved both sensitivity and specificity.  Paper 2:           Despite some striking differences in profiles between Europe and the USA, the most important risk factors for >50% stenosis in both groups were male gender followed by diabetes. When the log CAC score was included as a risk factor, it became by far the most important predictor of >50% stenosis in both continents, followed by male gender. In the northern vs southern Europe comparison the result was similar, with the log CAC score being the most important predictor of >50% stenosis in both regions, followed by male gender.  Paper 3:           Independent predictors of CAC presence in males and females were age, dyslipidaemia, hypertension, diabetes and smoking, with the addition of family history of CAD in males; obesity was not predictive in either gender. The most important predictors of CAC presence in males were dyslipidaemia and diabetes, while among females the most important predictors of CAC presence were diabetes followed by smoking. When analysed by age groups, in both males and females aged <70 years, diabetes, hypertension and dyslipidaemia were predictive, with diabetes being the strongest; in females aged <70 years, smoking was also predictive. Among those aged ≥70 years, the results are completely different, with only dyslipidaemia being predictive in males but smoking and diabetes were predictive in females.  Paper 4:           In the total cohort, age, male gender, diabetes, obesity, family history of CAD and number of risk factors predicted an increasing CAC score, with the most important being male gender and diabetes. In males, hypertension and dyslipidaemia were also predictive, although diabetes was the most important predictor. Diabetes was similarly the most important risk factor in females, followed by age and number of risk factors. Among patients with CAC, hypertension, dyslipidaemia and diabetes predicted CAC extent in both males and females, with diabetes being the strongest predictor in males followed by dyslipidaemia, while diabetes was also the strongest predictor in females, followed by hypertension. Quantile regression confirmed the consistent predictive ability of diabetes.  Paper 5:           In the systematic review, age was strongly predictive of both CAC presence and extent but not of CAC progression. The results for CAC presence were overwhelmed by data from one study of almost 10,000 patients, which found that white ethnicity, diabetes, hypertension and obesity were predictive of CAC presence but not male gender, dyslipidaemia, family history or smoking. With respect to CAC extent, only male gender and hypertension were clearly predictive, while in the one study of CAC progression, only diabetes and hypertension were predictive. In the meta-analysis, hypertension followed by male gender, diabetes and age were predictive of CAC presence, while for CAC extent mild-moderate CAC was predicted by hypertension alone, whereas severe CAC was predicted by hypertension followed by diabetes.   Conclusion Our investigation of the Euro-CCAD cohort showed that the CAC score is far more predictive of significant stenosis than risk factors alone, followed by male gender and diabetes, and there was little benefit to risk factor assessment over and above the CAC score for >50% stenosis prediction. Regional variations made little difference to this result. Independent predictors of CAC presence were dyslipidaemia and diabetes in males and diabetes followed by smoking in females. The risk factor predictors alter at age 70. The most important risk factor predictors of CAC extent were male gender and diabetes; when analysed by gender, diabetes was the most important in both males and females. Our studies have consistently shown the strong predictive ability of male gender in the total cohort and diabetes in males and females and this is reflected in the meta-analysis, which also found hypertension to be independently predictive. Interestingly, dyslipidaemia does not appear to be a strong risk factor.
APA, Harvard, Vancouver, ISO, and other styles
10

Sjögren, Per. "Cardiovascular risk factors, diet and the metabolic syndrome /." Stockholm, 2006. http://diss.kib.ki.se/2006/91-7140-894-0/.

Full text
APA, Harvard, Vancouver, ISO, and other styles
More sources

Books on the topic "Atherosclerosis – Risk factors"

1

Maciejko, James J. Atherosclerosis Risk Factors. Washington, DC: AACC Press, 2004.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
2

M, Grundy Scott, and Current Medicine Inc, eds. Atlas of atherosclerosis. 4th ed. Philadelphia: Current Medicine, 2005.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
3

1948-, Wilson Peter, and Current Medicine Inc, eds. Atlas of atherosclerosis: Risk factors and treatment. 3rd ed. Philadelphia: Current Medicine, 2003.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
4

Tousoulis, Dimitris. Risk factors and vascular endothelium. Hauppauge, N.Y: Nova Science Publishers, 2011.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
5

Zhang, Xiao-hua. Investigations of effects of garlic materials upon risk factors of atherosclerosis. Wolverhampton: University of Wolverhampton, 2000.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
6

Schettler, Gotthard, ed. Endemic Diseases and Risk Factors for Atherosclerosis in the Far East. Berlin, Heidelberg: Springer Berlin Heidelberg, 1988. http://dx.doi.org/10.1007/978-3-642-83358-8.

Full text
APA, Harvard, Vancouver, ISO, and other styles
7

Yeagle, Philip. Understanding your cholesterol. San Diego: Academic Press, 1991.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
8

Yeagle, Philip. Understanding your cholesterol. San Diego: Academic Press, 1991.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
9

M, Gotto Antonio, ed. Multiple risk factors in cardiovascular disease. Dordrecht: Kluwer Academic Publishers, 1992.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
10

Frank, Clifford R. Pediatric prevention of atherosclerotic cardiovascular disease. New York: Oxford University Press, 2006.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
More sources

Book chapters on the topic "Atherosclerosis – Risk factors"

1

Minematsu, Kazuo, Oh Young Bang, and Toshiyuki Uehara. "Risk Factors." In Intracranial Atherosclerosis, 45–54. Oxford, UK: Wiley-Blackwell, 2009. http://dx.doi.org/10.1002/9781444300673.ch4.

Full text
APA, Harvard, Vancouver, ISO, and other styles
2

Haverich, Axel, and Erin Colleen Boyle. "Atherosclerosis Risk Factors." In Atherosclerosis Pathogenesis and Microvascular Dysfunction, 9–45. Cham: Springer International Publishing, 2019. http://dx.doi.org/10.1007/978-3-030-20245-3_2.

Full text
APA, Harvard, Vancouver, ISO, and other styles
3

Wilson, Peter W. F. "The Newer Coronary Risk Factors." In Atlas of Atherosclerosis, 179–91. London: Current Medicine Group, 2000. http://dx.doi.org/10.1007/978-1-4757-9310-9_10.

Full text
APA, Harvard, Vancouver, ISO, and other styles
4

Krumholz, Harlan M., and Lee Goldman. "Cost-Effectiveness of Risk Factors." In Atlas of Atherosclerosis, 237–50. London: Current Medicine Group, 2000. http://dx.doi.org/10.1007/978-1-4757-9310-9_13.

Full text
APA, Harvard, Vancouver, ISO, and other styles
5

Wilson, Peter W. F. "The Newer Coronary Risk Factors." In Atlas of Atherosclerosis, 193–211. London: Current Medicine Group, 2003. http://dx.doi.org/10.1007/978-1-4615-6484-3_10.

Full text
APA, Harvard, Vancouver, ISO, and other styles
6

Heidenreich, Paul A., and Harlan M. Krumholz. "Cost-Effectiveness of Risk Factors." In Atlas of Atherosclerosis, 259–72. London: Current Medicine Group, 2003. http://dx.doi.org/10.1007/978-1-4615-6484-3_13.

Full text
APA, Harvard, Vancouver, ISO, and other styles
7

Wenger, Nanette K. "Gender Differences in Coronary Risk Factors and Risk Interventions." In Atlas of Atherosclerosis, 213–36. London: Current Medicine Group, 2000. http://dx.doi.org/10.1007/978-1-4757-9310-9_12.

Full text
APA, Harvard, Vancouver, ISO, and other styles
8

Wenger, Nanette K. "Gender Differences in Coronary Risk Factors and Risk Interventions." In Atlas of Atherosclerosis, 235–58. London: Current Medicine Group, 2003. http://dx.doi.org/10.1007/978-1-4615-6484-3_12.

Full text
APA, Harvard, Vancouver, ISO, and other styles
9

Khera, Amit. "History of the Evolution of Cardiovascular Risk Factors and the Predictive Value of Traditional Risk-Factor-Based Risk Assessment." In Asymptomatic Atherosclerosis, 89–105. Totowa, NJ: Humana Press, 2010. http://dx.doi.org/10.1007/978-1-60327-179-0_7.

Full text
APA, Harvard, Vancouver, ISO, and other styles
10

Chait, Alan, and Michael E. Rosenfeld. "Dietary Effects on Cardiovascular Risk Factors." In Atlas of Atherosclerosis, 127–54. London: Current Medicine Group, 2000. http://dx.doi.org/10.1007/978-1-4757-9310-9_8.

Full text
APA, Harvard, Vancouver, ISO, and other styles

Conference papers on the topic "Atherosclerosis – Risk factors"

1

Du, J. "AB0674 Risk factors of atherosclerosis in patients with takayasu’s arteritis." In Annual European Congress of Rheumatology, EULAR 2018, Amsterdam, 13–16 June 2018. BMJ Publishing Group Ltd and European League Against Rheumatism, 2018. http://dx.doi.org/10.1136/annrheumdis-2018-eular.3300.

Full text
APA, Harvard, Vancouver, ISO, and other styles
2

Long, David S., Hui Zhu, and Morton H. Friedman. "Quantifying the Motion of Murine Epicardial Coronary Arteries." In ASME 2008 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2008. http://dx.doi.org/10.1115/sbc2008-192065.

Full text
Abstract:
Coronary artery atherosclerosis is a leading cause of morbidity and mortality in western societies. Atherosclerosis is a progressive fibroinflammatory disease identified by intimal thickening, the focal accumulation of lipids, fibrous elements, and cellular elements within the walls of large arteries. These lesions preferentially develop at arterial branches, the outer walls of bifurcations, and the inner walls of curved sections; the cause of this focal vasculopathy is not fully understood. It is, however, understood from epidemiological and clinical studies that individual susceptibility to the development and progression of atherosclerotic lesions is influenced by “traditional” systemic risk factors, including smoking, diabetes mellitus, obesity, hypertension, and high cholesterol. However, these risk factors cannot account for half of the variability in occurrence of this disease; this indicates additional risk factors have not been identified. One prevalent explanation of the focal nature of the disease is that the local fluid mechanical stresses at the walls of coronary arteries, as well as mechanical stresses within the vessel wall, may mediate the phenotype of endothelial cells thereby producing atherosusceptible sites. Therefore, it has been speculated [1] that certain aspects of arterial geometry and motion, which vary substantially among individuals, may increase an individual’s susceptibility to developing atherosclerosis — “geometric risk factors”.
APA, Harvard, Vancouver, ISO, and other styles
3

Xie, Jiang, Haitao Wang, Jiyuan Zhang, Chao Meng, Yanyan Kong, Shanping Mao, Lingyu Xu, and Wu Zhang. "A novel hybrid subset-learning method for predicting risk factors of atherosclerosis." In 2017 IEEE International Conference on Bioinformatics and Biomedicine (BIBM). IEEE, 2017. http://dx.doi.org/10.1109/bibm.2017.8217987.

Full text
APA, Harvard, Vancouver, ISO, and other styles
4

Gerasimova, Helen, Tatiana Popkova, Olga Fomicheva, Lev Krougly, Svetlana Glukhova, and Diana Novikova. "FRI0044 RISK FACTORS FOR CORONARY ARTERY ATHEROSCLEROSIS IN PATIENTS WITH RHEUMATOID ARTHRITIS." In Annual European Congress of Rheumatology, EULAR 2019, Madrid, 12–15 June 2019. BMJ Publishing Group Ltd and European League Against Rheumatism, 2019. http://dx.doi.org/10.1136/annrheumdis-2019-eular.4765.

Full text
APA, Harvard, Vancouver, ISO, and other styles
5

Ilic, Gordana Grujic, and Milorad Jerkan. "P143 Obesity in children and the accompanyng risk factors important for atherosclerosis." In 8th Europaediatrics Congress jointly held with, The 13th National Congress of Romanian Pediatrics Society, 7–10 June 2017, Palace of Parliament, Romania, Paediatrics building bridges across Europe. BMJ Publishing Group Ltd and Royal College of Paediatrics and Child Health, 2017. http://dx.doi.org/10.1136/archdischild-2017-313273.231.

Full text
APA, Harvard, Vancouver, ISO, and other styles
6

Kuryta, O., T. Lusynets, and O. Sirenko. "AB0352 Risk factors and subclinical atherosclerosis in rheumatoid arthritis females comorbid with hypertension." In Annual European Congress of Rheumatology, 14–17 June, 2017. BMJ Publishing Group Ltd and European League Against Rheumatism, 2017. http://dx.doi.org/10.1136/annrheumdis-2017-eular.5343.

Full text
APA, Harvard, Vancouver, ISO, and other styles
7

Van der Heiden, K., H. C. Groen, P. C. Evans, L. Speelman, F. Gijsen, M. de Jong, A. F. W. van der Steen, and J. J. Wentzel. "Non-Invasive Molecular Imaging of Shear Stress-Induced Endothelial Activation and Atherosclerotic Plaque Vulnerability." In ASME 2012 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2012. http://dx.doi.org/10.1115/sbc2012-80515.

Full text
Abstract:
Atherosclerosis is a lipid- and inflammation driven disease of the larger arteries and is found at specific locations in the arterial tree, i.e. at branches and bends where endothelial cells are exposed to low and low, oscillatory shear stress. Shear stress, the frictional force acting on the endothelial cells as a result of the blood flow, affects endothelial physiology. It determines the location of atherosclerotic lesion development as low and low, oscillatory shear stress induce pro-inflammatory transcription factors but reduce expression and/or activity of anti-inflammatory transcription factors in endothelial cells, rendering the vascular wall vulnerable for inflammation. Consequently, in the presence of atherosclerotic risk factors, such as hypercholesterolemia and diabetes, atherosclerotic lesion development can occur. Although the relationship between low and low, oscillatory shear stress and the prevalence of atherosclerosis has been recognized for several decades, insight into the mechanisms underlying this relationship is still incomplete. The correlation between shear stress and endothelial inflammation was demonstrated by in vitro experiments, in which cultured endothelial cells were exposed to specific flow profiles, and confirmed in vivo by gene expression pattern studies at atherosclerosis-susceptible sites. However, the relationship was not substantiated by direct causal in vivo evidence. Therefore, we developed a method to change the local shear stress field in mice in vivo and studied its effect on the endothelial molecular pathways and resulting atherosclerotic plaque formation. Moreover it allowed us to develop non-invasive molecular imaging strategies to detect vulnerable plaques.
APA, Harvard, Vancouver, ISO, and other styles
8

Sirenko, Oksana, Olexandr Kuryata, and Tetyana Lysunets. "FRI0730-HPR CAROTID ATHEROSCLEROSIS AND CARDIOVASCULAR RISK FACTORS IN FEMALES WITH SYSTEMIC LUPUS ERYTHEMATOSUS." In Annual European Congress of Rheumatology, EULAR 2019, Madrid, 12–15 June 2019. BMJ Publishing Group Ltd and European League Against Rheumatism, 2019. http://dx.doi.org/10.1136/annrheumdis-2019-eular.2609.

Full text
APA, Harvard, Vancouver, ISO, and other styles
9

Knott, E. P., B. Zarrabian, L. Khalid, and N. Sinha. "The Effect of Donor Risk Factors for Atherosclerosis on Primary Graft Dysfunction After Lung Transplantation." In American Thoracic Society 2021 International Conference, May 14-19, 2021 - San Diego, CA. American Thoracic Society, 2021. http://dx.doi.org/10.1164/ajrccm-conference.2021.203.1_meetingabstracts.a1781.

Full text
APA, Harvard, Vancouver, ISO, and other styles
10

Doney, Brent, Eva Hnizdo, Monica Graziani, Greg Kullman, Cecil Burchfiel, Sherry Baron, Kaori Fujishiro, et al. "Occupational Risk Factors For Airflow Limitation In The Multi-Ethnic Study Of Atherosclerosis (MESA) Lung Study." In American Thoracic Society 2012 International Conference, May 18-23, 2012 • San Francisco, California. American Thoracic Society, 2012. http://dx.doi.org/10.1164/ajrccm-conference.2012.185.1_meetingabstracts.a3893.

Full text
APA, Harvard, Vancouver, ISO, and other styles
You might also be interested in the extended bibliographies on the topic 'Atherosclerosis – Risk factors' for particular source types:
Journal articles Dissertations / Theses Books
We offer discounts on all premium plans for authors whose works are included in thematic literature selections. Contact us to get a unique promo code!

To the bibliography